Effects of omega-3 fatty acids on intravascular lipolysis of very-low-density lipoproteins in humans

Siddika E Karakas, Revital Herrmann, Rogelio Almario

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Very-low-density lipoproteins (VLDLs) are the major carriers of fasting plasma triglyceride (TG). TG-enriched VLDLs become cholesterol (C)-enriched low-density lipoproteins (LDLs) through hydrolysis facilitated by lipoprotein lipase (LPL). Omega-3 fatty acid (n-3 FA) supplementation may increase LDL-C while decreasing plasma TG in hypertriglyceridemic patients. It has been proposed that n-3 FAs increase LDL-C by promoting production of TG-poor VLDL and accelerating conversion of VLDL to LDL. To study the effects of n-3 FA supplementation on in vivo lipolysis of VLDL directly, we treated 11 hypertriglyceridemic subjects with n-3 FA (3.3 g/d). Each participant was studied three times: at baseline, after a 1-month period of run-in olive oil placebo, and after 1 more month of n-3 FA supplementation. Lipolysis was induced by intravenous infusion of heparin for 2 hours. Plasma samples were obtained every 30 minutes for determination of lipids and apoproteins (apos), separation of individual lipoproteins by fast protein liquid chromatography (FPLC), and measurement of LPL and hepatic TG lipase (HTGL) levels. n-3 FA supplementation decreased fasting plasma TG (2.51 ± 0.23 v 3.97 ± 0.46 mmol/L), VLDL-TG (1.08 ± 0.18 v 2.35 ± 0.35 mmol/L), and VLDL-C (0.39 ± 0.05 v 0.72 ± 0.13 mmol/L) while increasing LDL-C (3.59 ± 0.21 v 3.00 ± 0.23 mmol/L) and plasma apo B (3.31 ± 0.19 v 2.90 ± 0.17 mmol/L). The absolute rate of TG lipolysis correlated with fasting TG (r = .74, P < .005) and was lower after n-3 FA supplementation (0.11 ± 0.01 mmol/mL/min) as compared with placebo (0.19 ± 0.01, P < .01), whereas percent decreases from baseline TG levels were similar at entry onto the study (57.4% ± 2.5%), after placebo (58.8% ± 2.7%), and after n-3 FA (52% ± 3.6%). During lipolysis, LDL-C increased in correlation with the decrease in VLDL-C (r = -.41, P < .03), consistent with the product-precursor relationship. Postheparin LPL activity at 2 hours correlated inversely with fasting TG (r = -.53, P < .05), but not with either the decreases in VLDL-TG and VLDL-C or the increase in LDL-C. These data demonstrate that n-3 FA supplementation does not accelerate lipolysis of VLDL and even decreases the VLDL-C pool, which is the precursor of LDL-C. Therefore, the increase seen in fasting LDL-C is probably mediated through mechanisms other than acceleration of VLDL lipolysis.

Original languageEnglish (US)
Pages (from-to)1223-1230
Number of pages8
JournalMetabolism
Volume44
Issue number9
DOIs
StatePublished - 1995

Fingerprint

VLDL Lipoproteins
Lipolysis
Omega-3 Fatty Acids
LDL Lipoproteins
Triglycerides
Fasting
Lipoprotein Lipase
Placebos
VLDL Cholesterol
Apoproteins
Apolipoproteins B
Lipase
Intravenous Infusions
Liquid Chromatography
Lipoproteins
Heparin
Hydrolysis
Lipids
Liver

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Effects of omega-3 fatty acids on intravascular lipolysis of very-low-density lipoproteins in humans. / Karakas, Siddika E; Herrmann, Revital; Almario, Rogelio.

In: Metabolism, Vol. 44, No. 9, 1995, p. 1223-1230.

Research output: Contribution to journalArticle

Karakas, Siddika E ; Herrmann, Revital ; Almario, Rogelio. / Effects of omega-3 fatty acids on intravascular lipolysis of very-low-density lipoproteins in humans. In: Metabolism. 1995 ; Vol. 44, No. 9. pp. 1223-1230.
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N2 - Very-low-density lipoproteins (VLDLs) are the major carriers of fasting plasma triglyceride (TG). TG-enriched VLDLs become cholesterol (C)-enriched low-density lipoproteins (LDLs) through hydrolysis facilitated by lipoprotein lipase (LPL). Omega-3 fatty acid (n-3 FA) supplementation may increase LDL-C while decreasing plasma TG in hypertriglyceridemic patients. It has been proposed that n-3 FAs increase LDL-C by promoting production of TG-poor VLDL and accelerating conversion of VLDL to LDL. To study the effects of n-3 FA supplementation on in vivo lipolysis of VLDL directly, we treated 11 hypertriglyceridemic subjects with n-3 FA (3.3 g/d). Each participant was studied three times: at baseline, after a 1-month period of run-in olive oil placebo, and after 1 more month of n-3 FA supplementation. Lipolysis was induced by intravenous infusion of heparin for 2 hours. Plasma samples were obtained every 30 minutes for determination of lipids and apoproteins (apos), separation of individual lipoproteins by fast protein liquid chromatography (FPLC), and measurement of LPL and hepatic TG lipase (HTGL) levels. n-3 FA supplementation decreased fasting plasma TG (2.51 ± 0.23 v 3.97 ± 0.46 mmol/L), VLDL-TG (1.08 ± 0.18 v 2.35 ± 0.35 mmol/L), and VLDL-C (0.39 ± 0.05 v 0.72 ± 0.13 mmol/L) while increasing LDL-C (3.59 ± 0.21 v 3.00 ± 0.23 mmol/L) and plasma apo B (3.31 ± 0.19 v 2.90 ± 0.17 mmol/L). The absolute rate of TG lipolysis correlated with fasting TG (r = .74, P < .005) and was lower after n-3 FA supplementation (0.11 ± 0.01 mmol/mL/min) as compared with placebo (0.19 ± 0.01, P < .01), whereas percent decreases from baseline TG levels were similar at entry onto the study (57.4% ± 2.5%), after placebo (58.8% ± 2.7%), and after n-3 FA (52% ± 3.6%). During lipolysis, LDL-C increased in correlation with the decrease in VLDL-C (r = -.41, P < .03), consistent with the product-precursor relationship. Postheparin LPL activity at 2 hours correlated inversely with fasting TG (r = -.53, P < .05), but not with either the decreases in VLDL-TG and VLDL-C or the increase in LDL-C. These data demonstrate that n-3 FA supplementation does not accelerate lipolysis of VLDL and even decreases the VLDL-C pool, which is the precursor of LDL-C. Therefore, the increase seen in fasting LDL-C is probably mediated through mechanisms other than acceleration of VLDL lipolysis.

AB - Very-low-density lipoproteins (VLDLs) are the major carriers of fasting plasma triglyceride (TG). TG-enriched VLDLs become cholesterol (C)-enriched low-density lipoproteins (LDLs) through hydrolysis facilitated by lipoprotein lipase (LPL). Omega-3 fatty acid (n-3 FA) supplementation may increase LDL-C while decreasing plasma TG in hypertriglyceridemic patients. It has been proposed that n-3 FAs increase LDL-C by promoting production of TG-poor VLDL and accelerating conversion of VLDL to LDL. To study the effects of n-3 FA supplementation on in vivo lipolysis of VLDL directly, we treated 11 hypertriglyceridemic subjects with n-3 FA (3.3 g/d). Each participant was studied three times: at baseline, after a 1-month period of run-in olive oil placebo, and after 1 more month of n-3 FA supplementation. Lipolysis was induced by intravenous infusion of heparin for 2 hours. Plasma samples were obtained every 30 minutes for determination of lipids and apoproteins (apos), separation of individual lipoproteins by fast protein liquid chromatography (FPLC), and measurement of LPL and hepatic TG lipase (HTGL) levels. n-3 FA supplementation decreased fasting plasma TG (2.51 ± 0.23 v 3.97 ± 0.46 mmol/L), VLDL-TG (1.08 ± 0.18 v 2.35 ± 0.35 mmol/L), and VLDL-C (0.39 ± 0.05 v 0.72 ± 0.13 mmol/L) while increasing LDL-C (3.59 ± 0.21 v 3.00 ± 0.23 mmol/L) and plasma apo B (3.31 ± 0.19 v 2.90 ± 0.17 mmol/L). The absolute rate of TG lipolysis correlated with fasting TG (r = .74, P < .005) and was lower after n-3 FA supplementation (0.11 ± 0.01 mmol/mL/min) as compared with placebo (0.19 ± 0.01, P < .01), whereas percent decreases from baseline TG levels were similar at entry onto the study (57.4% ± 2.5%), after placebo (58.8% ± 2.7%), and after n-3 FA (52% ± 3.6%). During lipolysis, LDL-C increased in correlation with the decrease in VLDL-C (r = -.41, P < .03), consistent with the product-precursor relationship. Postheparin LPL activity at 2 hours correlated inversely with fasting TG (r = -.53, P < .05), but not with either the decreases in VLDL-TG and VLDL-C or the increase in LDL-C. These data demonstrate that n-3 FA supplementation does not accelerate lipolysis of VLDL and even decreases the VLDL-C pool, which is the precursor of LDL-C. Therefore, the increase seen in fasting LDL-C is probably mediated through mechanisms other than acceleration of VLDL lipolysis.

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